Journal of clinical & laboratory immunology最新文献

{"title":"An informative case of Graves' disease with implications for schizophrenia.","authors":"D D Adams,&nbsp;J G Knight,&nbsp;P Manning,&nbsp;G Smith","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The aetiology of schizophrenia and the other psychoses is not yet established. The Knight model, based on genetic and other evidence, proposes that schizophrenia is an autoimmune disease, caused by the development of forbidden clones of B lymphocytes that secrete autoantibodies that accidentally stimulate cell surface receptors on certain neurons, affecting the limbic system of the brain. An unusual defect in a Maori man with Graves' disease rendered him unresponsive to the usually effective antithyroid drugs, prompting his being treated with prednisone, a non-specific immunosuppressant agent. This was highly successful, reducing the blood level of the causative thyroid-stimulating autoantibodies with reduction of thyroid hormone levels and thyroid gland size. Unfortunately, high dosage prednisone can be used for only a month, because of steroid toxicity. A research pathway to effective therapy of receptor-mediated autoimmune diseases, which probably include the psychoses, is now apparent. It involves finding the autoantibodies, then cloning of their antigenic targets, as has been done for Graves' disease. This will provide knowledge of the peptide sequences necessary for constructing therapeutic agents for selectively destroying the pathogenic forbidden clones. Meanwhile, usage of short-term therapy with prednisone could be helpful in the management of schizophrenia and should be explored.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"53 ","pages":"13-25"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26114054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Policy and science of FMD control: the stakeholders' contribution to decision making. A call for integrated animal disease management.","authors":"M Marshall,&nbsp;P Roger","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Effective control of foot-and-mouth disease (FMD)--prevention, surveillance and response--requires integrated animal disease management as a cooperative effort between stakeholders, scientists and decision makers, at all levels: local, national, regional and international. This paper suggests a process and outlines specific critical issues that need to be addressed in order to best use the science and technology that is available now and to develop new technologies that will lead to significant improvements. The overall objective is not to allow the disease or the disease control measures to damage, violate or destroy public health, the environment, or the economy, or to allow politics to drive disease control policies at the expense of the ethical relationship between man and animals. Critical issues of prevention, surveillance and response policies are examined, and specific recommendations are made to reduce the risk or effect of natural and deliberate introductions. For prevention: a) rapid portable diagnostics and provision of vaccines to control and eradicate the reservoirs of disease. b) alerts, leading to increased controls at borders, animal movement restrictions and biosecurity on farms. For surveillance: a) reporting of unusual symptoms, rapid diagnostics and identification of patterns. b) enhanced role of geographic information systems (GIS) linked to an IT system. c) collection, storage and sharing of disease information. For response policies: a) the role and implementation of stamping out and of vaccination. b) simulation exercises with stakeholder participation. For all aspects of FMD control, consideration should be given to: a) the composition, responsibilities and role of the balanced, permanently operational Expert Group in EU member states as specified in the EU FMD Directive. b) establishment of a balanced, permanently operational European Expert Group. c) establishment of both a European and an International FMD Task Force. Stakeholders need access to accurate, up-to-date, unbiased information about the science of disease control, how the technologies work and can be used, and an assurance that the technologies best fit for the required purpose will be used. Researchers need to work together to avoid duplications and gaps in their research and to recognise the benefit of new, and sometimes innovative, technologies. They also need feedback from stakeholders on the acceptability and best use of the technologies. A process to achieve these goals through an EU funded collaborative research project will be described.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"53 ","pages":"27-38"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26114053","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Increase of circulating CD8+CD57+ lymphocytes after measles infection but not after measles vaccination.","authors":"B Aronsson,&nbsp;M Troye-Blomberg,&nbsp;L Smedman","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Natural measles virus infection is recognised to induce immunosuppression, contributing to an increased susceptibility to other infections. A cell population that could be involved in this process is the CD8CD57 double-positive lymphocyte subset (CD8+CD57+), known to be significantly expanded in some viral infections, e.g. human immunodeficiency virus (HIV) infection. We therefore studied the level of CD8+CD57+ lymphocytes during measles infection and measles vaccination. Twenty-two measles patients were examined 5-57 days after the onset of fever and several months later. Healthy, age-matched controls were examined twice. Eleven children receiving measles-mumps-rubella (MMR) vaccination were examined before, 9-19 days and 5-9 months afterwards. Blood samples were analysed for the proportion of peripheral blood mononuclear cells carrying both CD8 and CD57, and for other cell surface markers (CD4, CD14, CD3, CD16(CD56) or CD20). Elevated proportions of CD8CD57 double-positive cells were found in the peripheral blood of children with natural measles early after infection (p < 0.05), whereas the proportion of other cell surface markers remained stable. No corresponding change in CD8+CD57+ lymphocytes was noted in MMR-vaccinated children or in healthy controls. Since CD8+CD57+ lymphocytes could be related to the immunosuppression seen in some viral infections, our finding of elevated CD8CD57 double-positive lymphocytes during acute measles infection would suggest that this population of lymphocytes is involved in measles-induced immunosuppression. The absence of an increase of CD8CD57 in children vaccinated with the conventional live attenuated measles vaccine, in contrast to children with natural measles infection, would thus indicate that the vaccine does not induce immunosuppression as measured in our in vitro system.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"53 ","pages":"1-12"},"PeriodicalIF":0.0,"publicationDate":"2004-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26113576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Review: immunomodulatory activity of pregnancy-associated plasma protein-A.","authors":"S G Zhabin,&nbsp;V S Gorin,&nbsp;N S Judin","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>This mini-review highlights the growing number of indications for the immunological importance of pregnancy-associated plasma protein-A (PAPP-A), which is a remote member of the alpha-macroglobulin plasma protein family. PAPP-A can bind a variety of cytokines and specifically cleave a binding protein for insulin-like growth factors, thereby serving as a modulator of cytokine activity. Important immune functions, such as lymphocyte proliferation response to alloantigens and lectins and expression of HLA-DR molecules are predominantly suppressed in vitro by PAPP-A. It is likely that the immunoregulatory properties of PAPP-A are very similar to that of alpha 2-macroglobulin. The experimental data allows us to suppose that PAPP-A serves to prevent the recognition of the fetus by the maternal immune system and to suppress locally the host's immune response to the tumour.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"52 ","pages":"41-50"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24464203","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antibodies to Acinetobacter bacteria and bovine brain peptides, measured in bovine spongiform encephalopathy (BSE) in an attempt to develop an ante-mortem test.","authors":"C Wilson,&nbsp;L E Hughes,&nbsp;T Rashid,&nbsp;A Ebringer,&nbsp;S Bansal","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Bovine spongiform encephalopathy (BSE) is a neurological disease of cattle. Antibody responses to Acinetobacter radioresistens and six other bacteria, as well as to bovine myelin basic protein and bovine neurofilaments were measured in 128 BSE positive animals, 63 BSE negative animals and 64 healthy control animals. Animals positive for BSE had the highest levels of antibodies to Acinetobacter radioresistens (p < 0.0001) and also autoantibodies to bovine myelin basic protein (p < 0.0001) and bovine neurofilaments (p < 0.0001). In an endeavour to develop an antemortem test for BSE, 12 different strains of Acinetobacter were further tested in a MAN (myelin-Acinetobacter-neurofilament) assay involving 28 BSE positive and 18 BSE negative animals and defined bovine brain peptides. Five out of the 12 Acinetobacter bacteria tested [Acinetobacter (sp3), A. haemolyticus (sp4), A. johnsonii (sp7), A. lwoffii (sp8) and Acinetobacter (sp9)] gave 100% sensitivity and 100% specificity for detecting BSE. The highest anti-bacterial antibody level compared to controls was obtained with A. johnsonii. Further field studies are required to determine the validity of the MAN assay in detecting animals affected with BSE.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"52 ","pages":"23-40"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24464201","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Principles of autoimmune disease: pathogenesis, genetics and specific immunotherapy.","authors":"D D Adams,&nbsp;J G Knight","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The immunity system has the daunting task of producing lymphocyte clones able to react with any pathogenic microbe, new or old, to defend against infectious disease. It cannot do this without occasionally producing a forbidden clone, Burnet's apt name for the pathogenic lymphocyte clones that cause the autoimmune diseases by accidentally reacting with a host antigen instead of an antigen on an invading microbe. Unfortunately, Burnet's insight has been lost by immunologists, for four decades. V genes code for the specificity of receptors for antigen on B and T lymphocytes. They change by the DNA sequence copying errors (somatic mutations) that create new clones during the lymphocyte cell divisions that occur in an immune response to microbial infection. These mutations are necessary for achievement of the higher affinity, between a lymphocyte clone and the microbe, that enables recovery from infectious disease. H genes code for histocompatibility antigens, major, minor and HY. These are peptides, which, unlike V gene products, are invariant throughout life. H genes dictate the immune repertoire by constantly deleting any nascent lymphocyte clone reactive with them. This protects, with imperfect success, against autoimmune disease arising from the V gene changes that produce forbidden clones. Microbial triggers cause an autoimmune disease by initiating a cascade of clonal development that produces a forbidden clone by unlucky somatic mutations in lymphocyte V genes, exemplified by group A streptococci triggering rheumatic fever and measles triggering encephalomyelitis. Specific immunotherapy will come from finding and targeting forbidden clones.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"52 ","pages":"1-22"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24464200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Downregulation of RNase L inhibitor correlates with upregulation of interferon-induced proteins (2-5A synthetase and RNase L) in patients with chronic fatigue immune dysfunction syndrome.","authors":"A Vojdani,&nbsp;P C Choppa,&nbsp;C W Lapp","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Chronic Fatigue Immune Dysfunction Syndrome (CFIDS) is a disorder characterized by debilitating fatigue associated with immunological abnormalities and cognitive impairments. The recently cloned RNase L Inhibitor (RLI) gene encodes a specific protein which is believed to regulate 2-5A synthetase and RNase L activity via the formation of a latent heterodimeric protein complex. In the present study, we investigated the levels of 2-5A synthetase, RNase L and RLI in patients with CFIDS as compared to healthy controls. Quantitative Competitive PCR (Q/C PCR) analysis showed a statistically significant decrease in RLI mRNA present in the peripheral blood lymphocytes (PBL) of patients with CFIDS (n = 25, mean = 569, S.E = 154) as compared to RLI mRNA level present in peripheral blood lymphocytes (PBL) of healthy controls (n = 15, mean = 2296, S.E = 506; p < 0.0001). The decrease in RLI mRNA in CFIDS individuals correlated directly with RLI and RLI: RNase L protein ratio while showing an inverse relationship to the 2-5A synthetase and RNase L activity. This RLI mRNA and protein deficiency in CFIDS patients may explain the increase in activity of RNase L found in CFIDS patients. The unidirectional decrease in RLI message and protein levels in CFIDS individuals may contribute to the destabilization of the latent RLI:RNase L heterodimeric protein complex, resulting in the excessive activation of RNase L shown in this study. The increased activation of RNase L may result in an increased cellular RNA turnover and subsequent inhibition of protein synthesis; thus resulting in general fatigue, myalgia muscle weakness and other symptomatologies shown in CFIDS patients. Furthermore, this data supports the hypothesis that the antiviral 2-5 oligoadenylate synthetase (2-5OAS) overexpression in individuals with CFIDS correlates with an increase in RNase L activity and with a decrease in RNase L inhibitor.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"50 1","pages":"1-16"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21061520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Soluble interleukin-2R alpha test kits measure different epitopes: sIL-2R alpha test kits comparison with a newly developed inhouse sIL-2R alpha sandwich ELISA.","authors":"K Kazim,&nbsp;G Wild,&nbsp;A Ward","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cytokines are a group of low molecular weight glycoproteins important in cellular signaling for various responses such as activation and proliferation. They separate the cellular responses into Th1 and Th2 pathways, where each pathway releases its own cytokine group. Interleukins are an important section of the cytokine group, and consist of a number of members with their respective receptors such as interleukin-2 and interleukin-2 receptor (IL-2 and IL-2R, respectively). In this study, a soluble interleukin-2 receptor (sIL-2R alpha) sandwich ELISA was developed and tested with different samples. This method was compared with commercial test kits that measure sIL-2R alpha molecule. The results showed that different kits measure different epitopes on this molecule.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"50 2","pages":"55-61"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21334832","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-soluble interleukin-2R alpha combinations measure different epitopes: comparison between different anti-sIL-2R alpha antibody combinations and a newly developed in-house sIL-2R alpha sandwich ELISA.","authors":"K Kazim,&nbsp;G Wild,&nbsp;A Ward","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Cytokines are a group of low molecular weight glycoproteins important in cellular signaling for various responses such as activation and proliferation. They separate the cellular responses into Th1 and Th2 pathways, where each pathway releases its own cytokine group. Interleukins are an important section of the cytokine group and consist of a number of members with their respective receptors such as interleukin-2 and interleukin-2 receptor (IL-2 and IL-2R, respectively). In this study, a soluble interleukin-2 receptor alpha (sIL-2R alpha) sandwich ELISA was developed and tested with different samples. This method was compared with other mono- and polyclonal antibodies that measure sIL-2R alpha molecule using the same subjects and recombinant sIL-2R alpha. The results showed that different antibody combinations measure different epitopes on the receptor molecule.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"50 1","pages":"17-25"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21061521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crossroads of the effects of cyclophosphamide pulse therapy for lupus nephritis--experience of 11 cases.","authors":"M Funauchi,&nbsp;S Ikoma,&nbsp;M Sugiyama,&nbsp;H Yu,&nbsp;M Ohno,&nbsp;K Kinoshita,&nbsp;K Hamada,&nbsp;A Kanamaru","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>In this study time for initial assessment of monthly intravenous cyclophosphamide (CP) pulse therapy is discussed for a better outcome with less complications. Eleven patients with lupus nephritis (LN) resistant to conventional therapy (serum creatinine level < or = 2.7 mg/dl) were given 500 mg/m2 of CP 7-9 times with an interval of one month. Urinary protein (Up) decreased in all patients after 3 courses of CP pulse therapy and kept similar levels thereafter. In one group of patients (n = 7), Up decreased to < 2 g/day after 3 courses, while in the other group (n = 4), it did not decrease to < 4 g/day. Creatinine clearance increased by 0-100% in the former group, while it decreased by 5-20% in the latter group after 6-9 courses. Renal function of the patients with insufficient response after 3 courses tended to show no further improvement or worsened thereafter, although Up decreased during CP pulse therapy. A relatively small dose of CP (500 mg/m2) pulse therapy was useful in most LN patients regardless of the renal histology and it was thought important to assess its effects after 3 courses for a prediction of the clinical course. Modification of the protocol at that time might be necessary in regard to dose or interval of CP administration especially for patients with insufficient outcome.</p>","PeriodicalId":75994,"journal":{"name":"Journal of clinical & laboratory immunology","volume":"50 2","pages":"45-54"},"PeriodicalIF":0.0,"publicationDate":"1998-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"21334831","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}